PMID- 8879188
OWN - NLM
STAT- MEDLINE
DCOM- 19961203
LR  - 20111117
IS  - 1044-1549 (Print)
IS  - 1044-1549 (Linking)
VI  - 15
IP  - 4
DP  - 1996 Oct
TI  - Contrasting response of lung parenchymal cells to instilled TNF alpha and IFN 
      gamma: the inducibility of specific cell ICAM-1 in vivo.
PG  - 540-50
AB  - Induction of intercellular adhesion molecule-1 (ICAM-1) by proinflammatory 
      cytokines during inflammation plays an important role in regulating 
      polymorphonuclear neutrophil (PMN) migration and localization. In this report, we 
      examined the effects of tumor necrosis factor-alpha (TNF alpha) and 
      interferon-gamma (IFN gamma) on specific lung cell expression of ICAM-1 in vivo 
      and the accompanying morphological changes. Balb-c mice were treated with 
      phosphate-buffered saline (PBS) alone or with PBS containing 5 micrograms TNF 
      alpha or IFN gamma through intranasal instillation. Twenty-four hours after 
      treatment, their lungs were processed for immunoblot analysis and electron 
      microscope immunocytochemistry. In the normal lung, the ICAM-1 level is high on 
      type I alveolar epithelial cells, medium on arterial and venous endothelial 
      cells, low on type II epithelial cells and capillary endothelium, and not 
      detectable on bronchial epithelium. Topical treatment of the lung with either TNF 
      alpha or IFN gamma induced a 50-60% increase in total lung and alveolar ICAM-1. A 
      dramatic increase of alveolar type II cell surface ICAM-1 was observed (> 
      20-fold). Both cytokines caused 2-3-fold higher ICAM-1 expression on capillary 
      endothelial cells and a 40% increase of ICAM-1 on alveolar type I cells that was 
      not uniform. However, due to the large total surface area of type I epithelium, 
      type I cells contribute 70-86% of total alveolar septal ICAM-1 and > 90% of 
      alveolar surface ICAM-1 in either treated or normal mouse lungs. Increased ICAM-1 
      expression was also observed on nonparenchymal endothelial and epithelial cells. 
      Margination and sequestration of PMN in cytokine-treated lungs were observed by 
      histologic examination, measurements of total lung myloperoxidase activity, and 
      number of neutrophils recovered in bronchoalveolar lavage fluid. These results 
      showed that TNF alpha and IFN gamma induce ICAM-1 expression and infiltration of 
      neutrophils in the lung. The response of specific lung cells in terms of 
      induction of ICAM-1 in response to cytokine stimulation varied significantly, 
      particularly between type I and type II epithelial cells.
FAU - Kang, B H
AU  - Kang BH
AD  - Department of Cell Biology, Duke University Medical Center, Durham, North 
      Carolina, USA.
FAU - Manderschied, B D
AU  - Manderschied BD
FAU - Huang, Y C
AU  - Huang YC
FAU - Crapo, J D
AU  - Crapo JD
FAU - Chang, L Y
AU  - Chang LY
LA  - eng
GR  - P01 HL31992/HL/NHLBI NIH HHS/United States
GR  - R01 HL42609/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Administration, Intranasal
MH  - Animals
MH  - Immunoblotting
MH  - Intercellular Adhesion Molecule-1/*biosynthesis
MH  - Interferon-gamma/*administration & dosage
MH  - Lung/*metabolism/ultrastructure
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Microscopy, Immunoelectron
MH  - Recombinant Proteins
MH  - Tumor Necrosis Factor-alpha/*administration & dosage
EDAT- 1996/10/01 00:00
MHDA- 1996/10/01 00:01
CRDT- 1996/10/01 00:00
PHST- 1996/10/01 00:00 [pubmed]
PHST- 1996/10/01 00:01 [medline]
PHST- 1996/10/01 00:00 [entrez]
AID - 10.1165/ajrcmb.15.4.8879188 [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 1996 Oct;15(4):540-50. doi: 
      10.1165/ajrcmb.15.4.8879188.